Burstein Rami, Blake Pamela, Schain Aaron, Perry Carlton
aDepartment of Anesthesia, Critical Care, and Pain Medicine, Beth Israel Deaconess Medical Center bDepartment of Anesthesia, Harvard Medical School, Boston, Massachusetts cHeadache Center of Greater Heights, Memorial Hermann Medical Group dRiver Oaks Plastic Surgery Center, Houston, Texas, USA.
Curr Opin Neurol. 2017 Jun;30(3):263-271. doi: 10.1097/WCO.0000000000000437.
To summarize recent clinical and preclinical studies on extracranial pathophysiologies in migraine. It challenges the opinion-based notion that the headache phase of migraine occurs without input from peripheral nociceptors or is caused solely by activation of intracranial nociceptors supplying dural and cerebral vasculature.
Data that support a scenario by which migraine can originate extracranially include the perception of imploding headache that hurts outside the cranium, the existence of a network of sensory fibers that bifurcate from parent axons of intracranial meningeal nociceptors and reach extracranial tissues such as periosteum and pericranial muscles by crossing the calvarial bones through the sutures, the discovery of proinflammatory genes that are upregulated and anti-inflammatory genes that are down regulated in extracranial tissue of chronic migraine patients, and evidence that administration of OnabotulinumtoxinA to peripheral tissues outside the calvaria reduces frequency of migraine headache.
These findings seeks to shift clinical practice from prophylactically treating chronic migraine solely with medications that reduce neuronal excitability to treating irritated nociceptors or affected tissues. The findings also seeks to shift current research from focusing solely on central nervous system alterations and activation of meningeal nociceptors as a prerequisite for studying migraine.
总结近期关于偏头痛颅外病理生理学的临床和临床前研究。这对基于观点的观念提出了挑战，即偏头痛的头痛期在没有外周伤害感受器输入的情况下发生，或者仅由供应硬脑膜和脑血管的颅内伤害感受器激活引起。
支持偏头痛可起源于颅外的证据包括对颅骨外疼痛的爆裂样头痛的感知、从颅内脑膜伤害感受器的母轴突分叉并通过缝线穿过颅骨到达颅外组织（如骨膜和颅周肌肉）的感觉纤维网络的存在、慢性偏头痛患者颅外组织中上调的促炎基因和下调的抗炎基因的发现，以及向颅骨外周围组织注射A型肉毒毒素可降低偏头痛头痛频率的证据。
这些发现旨在将临床实践从仅用降低神经元兴奋性的药物预防性治疗慢性偏头痛转变为治疗受刺激的伤害感受器或受影响的组织。这些发现还旨在将当前的研究从仅关注中枢神经系统改变和脑膜伤害感受器激活作为研究偏头痛的先决条件上转移开来。
